| Title | Hepatitis C Virus Core Protein Sensitizes Cells to Apoptosis Induced by Anti-Cancer Drug |
|---|---|
| Author | Kang, Mun Il · Cho, Mong¹ · Kim, Sun Hee² · Kang, Chi Dug² · Kim, Dong Wan * |
| Address | Department of Microbiology, College of Natural Sciences, Chang Won National University; ¹Department of Medicine and ²Department of Biochemistry, College of Medicine, Pusan National University |
| Bibliography | Journal of Microbiology, 37(2),90-96, 1999, |
| DOI | |
| Key Words | Apoptosis, hepatitis C virus, core protein, anti-cancer drug |
| Abstract | The core protein of the hepatitis C virus (HCV) is a multifunctional protein. The HCV core protein was reported to regulate cellular gene expression and transform primary rat embryo fibroblast cells. However, the role of the core protein in the pathogenesis of HCV-associated liver diseases is not well understood. To investigate the functional role of the core protein in cytophathogenicity, we have constructed stable expression systems of full length or truncated HCV core protein lacking the C-terminal hyderophobic domains and established HepG2 cell clones constitutively expressing the core protein. The full length core protein was localized in the cytoplasm and the C-terminal truncated core protein was localized in the nucleus. HepG2 cells expressing nuclear, truncated core protein showed elevated cell death during cultivation compared to untransfected cells and full length core-expressing cells. In the treatment with bleomycin, both cell clones expressing full length or truncated core protein appeared to be more sensitive to bleomycin than the parental HepG2 cells. These results suggest that the core protein may play a role in HCV pathogenesis promoting apoptotic cell death of infected cells. |
| Download PDF | Eng_370207_90-96p.pdf |